In a groundbreaking finding, a new medicine Galvus (vildagliptin) has been created for people with type 2 diabetes that would lower blood glucose levels without the side effects of other medications.
1.5 million Australians are affected by type 2 diabetes and of these about 750,000 have been diagnosed. Type 2 diabetes involves complex pathologies. In type 1 diabetes no insulin is produced. In type 2 diabetes some insulin is produced but it is insufficient to enable glucose to move from the blood stream into the body cells and liver. As a result the blood sugar remains high.
Dr Gary Deed, Director of Diabetes Australia, Queensland explained, “The condition is commonly monitored with a glucose-lowering tablet, diet, exercise, and sometimes insulin.” He warned that inadequate sugar control over long term may lead to a host of complications including heart attack, stroke, nerve damage, kidney disease and blindness. He said weight gain is another link in these diabetics. “Research shows a lot of people (with type 2 diabetes) find weight control is an issue, and that certain medications contributed to weight gain,” he said.
The new medicine, Glavus, will lower blood sugar effectively without increasing body weight. Prof Greg Fulcher, director of diabetes services at Sydney's Royal North Shore Hospital explained that this medicine will “significantly increase” the likelihood of diabetes 2 patients reaching blood glucose targets of less than seven per cent. “Together, the clinical effectiveness and good tolerability of Galvus reinforce its potential for helping patients with type 2 diabetes and their doctors to better manage this chronic disease,” he said. These tablets would be taken once or twice in a day. The details of the treatment are to appear on the Pharmaceutical Benefits Scheme from August 1.
While the drug is still not approved for use in the US, it was approved in Feb 2008 by European Medicines Agency for use within the EU.
Effect of insulin on Bones
In two recent studies the role of the hormone insulin on bones has been explored. Insulin is a blood sugar regulating hormone that is deficient or absent in diabetics.
The studies published online July 22 in Cell, researchers have shown that insulin stimulates both bone building and breakdown in mice through the hormone's effects on two types of bone cells: bone-building osteoblasts and bone-resorbing osteoclasts. These cells are a part of continuous breakdown and rebuilding of our bones – a process called bone remodelling. The mechanism is thus a complex one. These bone cells in turn affect not only insulin production, but also blood sugar levels and energy metabolism. The bone cells have distinct insulin receptors that make the hormone function say researchers. To put it simply, the bony skeleton plays a role as regulator of whole-body energy metabolism like other metabolic regulators such as muscle and fat. This has important implications in treatment and research in type 2 diabetes and osteoporosis.
Researchers led by Thomas Clemens of Johns Hopkins University School of Medicine engineered mice so that their osteoblasts or bone forming cells no longer displayed insulin receptors. These mice developed a bone-making deficiency, having thinner bones with fewer osteoblasts. Their results suggest that insulin is necessary for mice to maintain normal bone mass. Dr. Clemens pointed out that type 1 diabetics who do not have insulin frequently have low bone mass, suggesting that the results may be relevant for humans. The team also found that these mice gained weight as they aged- a phenomenon not related to eating. In time they developed resistance to insulin – a condition seen in type 2 diabetics. The weight gain explains Clemens could be related to the bone hormone osteocalcin. “The reason these mice are fat is because they're not making enough insulin, which is because they're not making osteocalcin,” Clemens says. To confirm this, the researchers gave the insulin receptor-deficient mice osteocalcin, which improved their metabolic abnormalities.
In the second study led by Gerard Karsenty of Columbia University, insulin stimulates osteoblasts to produce an “inactive” form of osteocalcin that “sticks” to bone and doesn't enter circulation to stimulate the pancreas to secrete more osteocalcin. This inactive osteocalcin then erodes the bone with the help of osteoclasts. This explains the bone depletion process. Bone depletion or resorption the team found was linked to insulin secretion. “The significance of this is that bone is an integrated part of how whole body glucose equilibrium is regulated. Drugs that inhibit bone resorption [which are commonly used to treat osteoporosis] may, in certain patients, favor glucose intolerance,” Karsenty says. He adds that this is a concern that also needs to be addressed in future studies.
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